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Long Non-Coding RNA JPX Contributes to Tumorigenesis by Regulating miR-5195-3p/VEGFA in Non-Small Cell Lung Cancer
| Content Provider | Directory of Open Access Journals (DOAJ) |
|---|---|
| Author | Guo B. Li G. Li X. Li J. Yuan C. Zhou C. |
| Abstract | Guanglian Li, Xinrui Li, Chao Yuan, Caifeng Zhou, Xinxin Li, Jinfang Li, Bin Guo Department of Oncology, The People’s Hospital of Shouguang, Weifang, People’s Republic of ChinaCorrespondence: Bin GuoDepartment of Oncology, The People’s Hospital of Shouguang, No. 1223, Jiankang Street, Shouguang, Shandong, 262700, People’s Republic of ChinaTel +86 536 5225033Email jiulao1544624863@126.comBackground: Lung cancer is the most frequently diagnosed cancer. Of all lung cancers, 80– 85% are verified as non-small-cell lung cancer (NSCLC). Just proximal to X-inactive specific transcript (JPX), functions as lncRNA, contributed to tumor progression and suggested a poor prognosis in NSCLC. However, the pathogenesis of JPX involved in NSCLC is still unclear.Methods: The expressions of JPX, miR-5195-3p, and Vascular endothelial growth factor A (VEGFA) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Proliferation, colony number, apoptosis, invasion, and migration were analyzed by Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, transwell, and wound healing assays, severally. The protein levels of VEGFA, E-cadherin, N-cadherin, and Vimentin were detected by Western blot assay. The interaction between JPX, miR-5195-3p and VEGFA was predicted by starBase, and then verified by the dual-luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull-down assay. The biological role of JPX on NSCLC tumor growth was assessed by the xenograft tumor model in vivo.Results: JPX and VEGFA were upregulated, and miR-5195-3p was downregulated in NSCLC. JPX induced proliferation, colony number, invasion, migration, epithelial–mesenchymal transition (EMT), and inhibited apoptosis of NSCLC cells. JPX is directly bound to miR-5195-3p. JPX regulated NSCLC cell proliferation, apoptosis and EMT by modulating miR-5195-3p. miR-5195-3p hindered NSCLC cells proliferation, EMT and accelerated apoptosis by directly targeting VEGFA. JPX silencing hindered the cell growth of NSCLC in vivo.Conclusion: JPX facilitated proliferation, colony number, invasion, migration, EMT, and repressed apoptosis by miR-5195-3p/VEGFA axis, offering a possible therapeutic strategy for NSCLC.Keywords: lncRNA JPX, miR-5195-3p, VEGFA, lung cancer, proliferation, apoptosis, EMT |
| Related Links | https://www.dovepress.com/long-non-coding-rna-jpx-contributes-to-tumorigenesis-by-regulating-mir-peer-reviewed-article-CMAR |
| e-ISSN | 11791322 |
| Journal | Cancer Management and Research |
| Volume Number | 13 |
| Language | English |
| Publisher | Dove Medical Press |
| Publisher Date | 2021-01-01 |
| Publisher Place | United Kingdom |
| Access Restriction | Open |
| Subject Keyword | Neoplasms. Tumors. Oncology. Including Cancer and Carcinogens Lncrna Jpx Mir-5195-3p Vegfa Lung Cancer Proliferation Apoptosis Emt |
| Content Type | Text |
| Resource Type | Article |
